People with hepatitis C who received interferon-based
treatment were less likely to develop Parkinson’s disease, a large study from
Taiwan has concluded. The results, published in JAMA Neurology, add to the evidence that hepatitis C is a risk
factor for developing Parkinson’s disease and that antiviral treatment may reduce
this risk, say the study authors.
Parkinson’s disease is a degenerative neurological condition
that leads to tremors, slowed movement and eventually to difficulties in
walking, standing and swallowing. The risk of developing Parkinson’s disease
increases with age and several epidemiological studies have shown that
hepatitis C infection increases the risk of developing Parkinson’s disease.
However, epidemiological studies have not looked at the impact
of antiviral treatment for hepatitis C on the incidence of hepatitis C. This is
a concern owing to reports of the emergence of Parkinson’s-like symptoms in
some people after they began interferon treatment for hepatitis C.
To clarify the relationship between hepatitis C, interferon-based
treatment and Parkinson’s disease, investigators in Taiwan looked in the National
Health Insurance Database for all people with hepatitis C. They sought to
identify all cases of Parkinson’s disease diagnosed more than six months after
completing treatment with interferon alpha and ribavirin, between January 2003
and December 2013.
To eligible for inclusion in the analysis, patients had to
be over 20 years of age, without liver cirrhosis or any serious liver disease,
dementia or Parkinson’s disease. People treated for less than 16 weeks or with
less than six months of follow-up were excluded. The investigators identified 188,152
eligible patients, of whom 39,989 had undergone treatment. The treated patients
were matched 1:1 with people from the untreated group by age, sex, comorbidities
The mean age of the study population was 52 years, 55% were
male and approximately 13% had diabetes.
The incidence and risk of developing Parkinson’s disease was
calculated at one year, three years and five years of follow-up. The incidence
of Parkinson’s disease was 1 per 1000 person-years in the treated group and 1.39
per 1000 person-years in the untreated group.
Although there was no difference in
the risk of developing Parkinson’s disease after one year or three years of
follow-up, a significant difference in risk was evident after five years of
follow-up. Treated people were around 25% less likely to have developed Parkinson’s
disease by this point (HR, 0.75; 95%CI, 0.59-0.96).
When analysed by sub-group, people using
calcium channel blockers who received interferon treatment had a more
substantial reduction in risk than those who did not use calcium channel
blockers (HRs of non-dCCBs and CCBs, 0.81 vs 0.44; P for interaction =
.02). Approximately 13% of treated and untreated patients were taking a calcium
channel blocker. Calcium channel blockers have been associated with a lower
risk of developing Parkinson’s disease in
the general population too.
The investigators say
that the results show that interferon treatment does not raise the risk of Parkinson’s
disease in people with hepatitis C. A 6-month course of interferon treatment is
unlikely to exert a protective effect five years later, they argue. Instead, they
argue that treatment may limit the direct neurotoxic effect of hepatitis C, by clearing
the virus from the brain.
But the investigators warn
that the long period over which Parkinson’s disease develops makes if difficult
to judge whether treatment with interferon prevents or arrests the development
of the condition. The study could not distinguish between people cured of
hepatitis C and those who did not respond to treatment. Nor does it provide any
information about the impact of direct-acting antivirals on the risk of
developing Parkinson’s disease.